The heart is a muscular organ that is covered by a fibrous sac known as the pericardium. The space between the pericardium and the muscular organ is called the pericardial space. The walls of the heart are substantially formed from muscle (the myocardium) that differs from either skeletal or smooth muscle. The heart comprises atria and ventricles, each of which is composed of layers of myocardium that are formed to encase the blood-filled chambers. In operation, when the walls of a chamber contract, they come together similar to a squeezing fist. This contraction of the cardiac muscle is triggered by depolarization of the muscle membrane. To operate properly, the muscle contractions should be coordinated.
If the muscle contractions are not coordinated within the ventricles, blood may be sloshed back and forth within the ventricular cavities instead of being ejected into the aorta and pulmonary arteries. Thus, the complex muscle masses forming the ventricular pumps should contract substantially simultaneously for efficient pumping.
The heart is able to achieve this coordination because of (a) the tight junctions formed between adjacent cardiac fibers (the fibers are joined end to end at structures known as intercalated disks, which provide the points or junctions) which allow action potentials to be transmitted from one cardiac cell to another; and (b) the specialized muscle fibers in certain areas of the heart which provide the conducting system for proper excitation of the heart. The specialized fibers are in contact with fibers of the cardiac muscles to form gap junctions, which permit passage of action potentials from one cell to another. The specialized conduction system is configured, in normal operation, to provide a rapid and coordinated spread of excitation.
Cardiac muscle cells are autorhythmic, i.e., capable of spontaneous, rhythmical self-excitation. The sinoatrial (SA) node is the normal pacemaker for the entire heart or smooth muscle, and it is from this region that the excitation wave starts; it then moves or propagates through the remainder of the myocardium in a synchronized manner. The SA node region of the heart contains a small mass of specialized myocardial cells in the right atrial wall near the entrance of the superior vena cava that have a fast inherent rhythm, which allows the SA node to be the normal pacemaker. In unusual circumstances, other regions of the heart can become more excitable and provide a faster spontaneous rhythm. In this situation, this other region can become the pacemaker and the rhythm for the entire heart.
In normal operation, the cells of the SA node make contact with the surrounding atrial myocardium fibers. Thus, from the SA node, a wave of excitation spreads throughout the right atrium along the atrial myocardial cells via the gap junctions. In addition, the atrial tissue directs the impulse from the SA node directly to the left atrium, to simultaneously contract both atria.
The excitation wave then is distributed to the ventricles by way of a second small mass of specialized cells located at the base of the right atrium near the wall between the ventricles (the atrioventricular (AV) node). The AV node is configured to delay the propagation of action potentials (the wavefront) by about 0.1 second, to allow the atria to contract and empty the blood into the ventricle before ventricular contraction. The wavefront is then quickly dispersed along the specialized conducting fibers (down the interventricular septum to the ventricular free walls) and then through unspecialized (typical) myocardial fibers in the remaining myocardium.
The pumping of blood includes alternate periods of contraction and relaxation. The cardiac muscle has a relatively long refractory period (on the order of about 250 ms in humans). This refractory period is a time during which the membrane is insensitive to stimulus (either totally unable to propagate an excitation wave or only able to do so upon exposure to an increased level of stimulation).
Heart function may be decreased in certain conditions in heart failure. In such conditions, it may be possible to increase synchronization of electrical activity that increases the muscular contraction synchronization, thereby improving cardiac function.
During ventricullar fibrillation (VF) a number of independent activation wavefronts propagate simultaneously through the mycodardium. The propagation of these wavefronts may result in uncoordinated activity from the heart that may result in reduced or impaired cardiac function. Resuscitation attempts for cardiac arrest caused by VF include defibrillation shock. The defibrillation shock is intended to break up the propagation of the independent activation wavefronts to allow normal activation. If the fibrillation is halted by the first defibrillation shock applied to the affected area of the heart, no further action is typically required. If, on the other hand, the fibrillation is not halted by the first electric shock, the size of the shock is typically increased and a second defibrillation shock may be applied to the heart. Typically, this process is repeated until normal activity results. Three potentially problematic outcomes may result from application of a defibrillation shock. First, the defibrillation shock may fail to halt the fibrillation. Second, the defibrillation shock may halt the fibrillation but fibrillation may then re-occur in the next few seconds or minutes. Third, the defibrillation shock may be successful and cardiac electrical activity may return after the shock but cardiac function is either absent or greatly reduced. This third condition may be referred to as pulseless electrical activity (PEA).
The cause of atrial fibrillation or VF may be an indication of the strength of the defibrillation shock needed to halt the contraction of the heart muscle. For example, it is commonly thought that the defibrillation threshold, i.e. the strength of the defibrillation shock, is elevated when ventricular fibrillation occurs spontaneously in the presence of constriction and/or obstruction of a blood vessel (i.e. acute ischemia). Patients suffering from this condition will often have to be shocked using very high voltages. Exposing the heart muscle to these high voltages may damage the heart and cause persistent malfunction. The high voltage shocks may also lead to an arrhythmia of the heart or even death.
Thus, improvements may be needed in the treatment of fibrillation, either ventricular or atrial, that may reduce the occurrence of one or more of these problematic results. In particular, improvements may be needed to avoid damaging the heart.